Despite the prevalence of human vaginal trichomoniasis and the fact that Trichomonas vaginalis has been recognized as a pathogenic organism since 1916, little definitive information is available concerning parasite virulence factors and host immune factors that contribute to the establishment, maintenance, or elimination of genital trichomonad infections. Previous studies with this protozoan parasite have been limited by the lack of a suitable small animal model for genital trichomonad infection in which hypotheses developed from in vitro studies could be tested in vivo. The estrogenized BALB/c mouse will support chronic genital infections with the sexually transmitted trichomonad of bovines, Tritrichomonas foetus. Although estrogenized mice support chronic genital trichomonad infections, mice cured of infections or immunized with trichomonads display resistance to reinfection. The long- term objective of the proposed studies is to use this animal model of genital trichomoniasis to elucidate the role of host immune factors in the colonization and maintenance of genital trichomonad infections. The immediate objective of this study is to explore the role of trichomonad- specific IgG and secretory IgA antibodies in the colonization and maintenance of genital trichomoniasis in this model. The experimental design incorporates the use of a previously developed anti-T. foetus mouse monoclonal IgG library to develop mouse monoclonal secretory IgA antibodies to selected trichomonad surface membrane antigens and subsequently to characterize their molecular form, epitope specificities, and biologic activities. Purified mouse monoclonal secretory IgA and IgG antibodies of identical epitope specificities will be passively transferred into estrogenized normal or polymorphonuclear neutrophil- depleted BALB/c mice prior to or after establishment of genital trichomonad infections in order to define their roles in resistance to genital trichomoniasis. The specific aims established to achieve this objective are 1) to develop mouse monoclonal secretory IgA antibodies directed to selected trichomonad surface membrane antigens, 2) to use the estrogenized mouse model of genital trichomonad infection to examine the effect of passively transferred monoclonal secretory IgA and IgG antibodies on the establishment and maintenance of trichomonad infection, and 3) to use polymorphonuclear neutrophildepleted, estrogenized mice to examine the contribution of exudative polymorphonuclear neutrophils to resistance to trichomonad infection imparted by passively transferred mouse monoclonal antibodies.